Abstract | BACKGROUND: MATERIALS AND METHODS: Transgenic mice expressing human group IIA phospholipase A2 and their group IIA phospholipase A2 deficient nontransgenic C57BL/6 J littermates were infected with H. felis. The mice were killed 3, 8, and 19 weeks after inoculation of bacteria to determine the histopathological changes in gastric mucosa. RESULTS: The infected mice developed chronic inflammation in gastric mucosa. We found no differences in the colonization of bacteria between transgenic and nontransgenic mice. At 3 and 8 weeks, no difference was found in the severity of inflammation between the two groups. Nineteen weeks after the administration of bacteria the inflammation was more marked in nontransgenic than transgenic mice. Group IIA phospholipase A2 was expressed by in situ hybridization in the neck cells of the glandular stomach in transgenic mice. CONCLUSIONS:
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Authors | Heikki T Huhtinen, Juha M Grönroos, Jaakko Uksila, David S Grass, Timo J Nevalainen, V Jukka O Laine |
Journal | Helicobacter
(Helicobacter)
Vol. 9
Issue 5
Pg. 408-16
(Oct 2004)
ISSN: 1083-4389 [Print] England |
PMID | 15361079
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Phospholipases A
- Group II Phospholipases A2
- Phospholipases A2
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Topics |
- Animals
- Animals, Genetically Modified
- Chronic Disease
- Disease Models, Animal
- Gastric Mucosa
(enzymology, microbiology, pathology)
- Group II Phospholipases A2
- Helicobacter Infections
(enzymology, microbiology, pathology)
- Helicobacter felis
- In Situ Hybridization
- Mice
- Mice, Inbred C57BL
- Phospholipases A
(analysis, biosynthesis, blood)
- Phospholipases A2
- Time Factors
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